Pathogenic Features of Porphyromonas Gingivalis Influence Progression of Rheumatoid Arthritis

Abstract

Abstract Autoimmune diseases, such as rheumatoid arthritis (RA), are examples of yet not entirely understood etiology. They are linked to immune system dysfunction, which becomes immunologically overactive, damaging the body’s tissues and organs. At least three major factors underlie the development of autoimmune disorders: environmental factors, including the oral and intestinal microbiomes, genetic predisposition, and aberrant autoimmune response. The dysbiosis of the oral microbiota, in particular, exerts a significant effect on RA, clinically manifested by damage of the joints. RA is significantly associated with periodontitis, which is caused by an increased abundance of Porphyromonas gingivalis in the subgingival niche, which disturbs the homeostasis of the oral microbial community. P. gingivalis is considered to contribute to the development and progression of RA. Although this bacterium may escape detection by the host immune system, it still induces an immune imbalance. RA and periodontitis also share similar pathological and clinical features. The progression of both chronic periodontitis and RA is linked to the dysregulation of the immune system and the damage caused by the immune response. Previous detailed studies have indicated that a specific enzyme of P. gingivalis, peptidyl-arginine deiminase, which catalyzes the citrullination of proteins, may trigger the autoimmune response resulting in the development of RA.